<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Sartori C</dc:creator>
  <dc:creator>Rimoldi SF</dc:creator>
  <dc:creator>Rexhaj E</dc:creator>
  <dc:creator>Allemann Y</dc:creator>
  <dc:creator>Scherrer U</dc:creator>
  <dc:date>2016</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Epidemiological studies have shown an association between pathologic events occurring during early life and the development of cardiovascular and metabolic disease in adulthood. These observations have led to the so-called fetal programming of adult disease hypothesis. In line with this hypothesis, short-term exposure to hypoxia after birth predisposes to exaggerated hypoxic pulmonary vasoconstriction later in life in rats, and transient perinatal hypoxia predisposes to exaggerated pulmonary hypertension during short-term exposure to high altitude in humans. Along the same lines, in recent studies in Bolivian high-altitude dwellers, we found that preeclampsia predisposes the offspring to pulmonary and systemic endothelial dysfunction possibly related to impaired NO bioavailability and augmented oxidative stress. Very recent data from our lab suggest that assisted reproductive technologies may represent another important example consistent with this hypothesis. The mechanisms underpinning the developmental origin of this vascular dysfunction are poorly understood. Increasing evidence suggests that epigenetic alterations, such as DNA methylation or histone acetylation may play a role.</dc:description>
  <dc:identifier>https://sonar.ch/global/documents/57925</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1007/978-1-4899-7678-9_4</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/27343088</dc:relation>
  <dc:source>Advances in experimental medicine and biology. - 2016</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Endothelial function</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Epigenetic</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Hypoxia</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Preeclampsia</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Pulmonary hypertension</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Animals</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Cardiovascular Diseases</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Cardiovascular System</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Disease Models, Animal</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Environment</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">Epigenesis, Genetic</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Fetal Development</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">Humans</dc:subject>
  <dc:title xmlns:ns14="xml" ns14:lang="en">Epigenetics in Cardiovascular Regulation.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
